Lipid Droplet Biology and Fatty Liver
Fatty liver, also called hepatic steatosis, has become the most common disease of the liver in the United States. Over 40% of Americans have a fatty liver, which can lead to liver fibrosis, inflammation called hepatitis, cirrhosis and cancer. Moreover, because the liver is a central detoxification organ, it is especially susceptible to damage from alcohol. Most heavy drinkers exhibit fatty liver, referred to as ethanol-induced hepatic steatosis. And 40% to 50% of these people can develop severe, life-threatening disease. The central organelle within the hepatocyte that stores excess fat is the lipid droplet (LD). Scores of different proteins control the formation and utilization of LDs. A deficit in LD breakdown is believed to play a central role in fatty liver disease.
The Membrane Trafficking in Disease Lab's goals are to define how:
- The hepatocyte targets different catabolic proteins to the LD surface to mediate LD breakdown.
- The mechanisms by which autophagolysosomes engulf LDs in a process, termed lipophagy, mediate catabolism.
- The mechanisms by which LDs-autophagolysosomes-mitochondria interact to expedite lipid catabolism.
- Alcohol alters LD composition, function and breakdown.
- Alcohol alters the association of LD-bound proteins that can contribute to normal fat catabolism and autophagy.